S1M3 Introduction to Cardiovascular Pharmacology

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What is the first line of therapy for hypertension?

Diuretics, Thiazide-type,

Hydrochlorothiazide

What is the MOA of hydrochlorothiazide (a thiazide diuretic)?

Inhibits sodium reabsorbtion in the distal tubules leading to Na and water lost (as well as K+ and H++)

What is the Therapeutic use of Hydrochlorothiazide(a thiazide diuretic)?

Therapeutic use: For

mild to moderate hypertension or in combination withother drugs if hypertension is severe

What is the most common adverse effect of the use of Hydrochlorothiazide(a thiazide diuretic)?

Potassium depletion i.e. hypokalemia.

Dangerous in patients taking digitalis (increases contractility), in patients with chronic arrhythmias, and in acute MI

What are the pharmacokinetics of Hydrochlorothiazide (a thiazide diuretic)?

Onset

of action (i.e. diuresis) ~ 2

hours

Peak

effect: 4-6 hours

Duration

of action: 6-12 hours

Absorption: ~ 50% - 60%

Distribution: 3.6 – 7.8 L / Kg

Protein

binding: 68%

Metabolism: Not metabolized

Bioavailability: 70%

Half-life

of elimination: 5.6 – 14.8 hours

Time

to peak effect: 1 – 2.5 hours

Excretion; Urine (as unchanged drug)

A patient of African descent tends to retain sodium---would it be ok to give them Hydrochlorothiazide?

Yes, because it inhibits sodium reabsorption in the distal tubules leading to Na and water loss (and K+ and H+ loss, which is why you don't want to give this thiazide diuretic to anyone who has hypokalemia or is taking digitalis)

What is one example of an Angiotensin Converting Enzyme Inhibitor (ACEIs)?

It is caused by a chronic narrowing of coronary arteries due to atherosclerosis.

This narrowing is readily observed in the large epicardial arteries by coronary angiography.

What is Unstable Angina?

Avery dangerous type of angina that predisposes the individual to a high risk of myocardial infarction.

Unstable angina is caused by transient formation and dissolution of a blood clot within a coronary artery.

The clots often form in response to plaque rupture in atherosclerotic coronary arteries; however, the clot may also form because diseased coronary artery endothelium is unable to produce nitric oxide and prostacyclin that inhibit platelet aggregation and clot formation.